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First published on April 4, 2006; DOI: 10.1124/mol.105.021998

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Received for publication January 3, 2006.
Revised April 3, 2006.
Accepted for publication April 4, 2006.

RECEPTOR REGULATION OF AXON GUIDANCE MOLECULE GENE EXPRESSION

Amy K. Jassen 1, Hong Yang 2, Gregory M Miller 2, Elizabeth Calder 3, Bertha K. Madras 3*

1 Harvard Medical School,New England Primate Research Center 2 Harvard Medical School, New England Primate Research Center 3 Harvard Medical School/New England Primate Research Center

* Address correspondence to: E-mail: bertha_madras{at}hms.harvard.edu

Abstract

Axon guidance molecules, critical for neurodevelopment, are also implicated in morphological and other neurodaptative changes mediated by physiological or pharmacological events in adult brain. As an example, the psychostimulant cocaine markedly alters axon guidance molecules in adult brain of cocaine-treated rats. To decipher a potential link between drug-induced activation of G-protein coupled receptors (GPCRs) and modulation of axon guidance molecules, we investigated whether GPCR activity in a SK-N-MC human neuroepithelioma cell line (which expresses low levels of D1 dopamine receptors) affects gene expression of axon guidance molecules (semaphorins, ephrins, netrins and their receptors). Using real time PCR, we identified 17 of 26 axon guidance molecules in these cells, with varying levels of expression. Forskolin, which raised intracellular cAMP levels 340%, increased EphA5, EphB2 and Neuropilin1 expression, paralleling reported changes in the rat hippocampus after cocaine treatment. The dopamine receptor agonist dihydrexidine, which raised cAMP levels 22%, promoted regulatory changes in EphrinA1, EphrinA5, EphB1, DCC and Semaphorin3C, whereas SKF 81297 altered EphA5, EphrinA1 EphrinA5 and neuropilin1. cAMP and other signal transduction pathways may regulate axon guidance molecule gene expression, potentially linking monoamine receptor activation to signal transduction cascades, transcriptional regulation of axon guidance molecules and alterations in neural networks.


Key words: Dopamine, cAMP, CREB, Regulation of gene expression, Cocaine, Synaptic plasticity


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